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Association of influenza with congenital tracheoesophageal fistula and oesophageal atresia: an analysis of clusters

N. C.
Doc.
J-£ NORTH CAROLINA STATE LIBRARY
40?/<3:S4 RALEIGH
" PHSB STUDIES — A Special Report Series by the N,C. Department of Human Resources, Division of
Health Services, Public Health Statistics Branch, P.O. Box 2091, Raleigh, N.C.
No. ]k March 1979
ASSOCIATION OF INFLUENZA WITH CONGENITAL
TRACHEOESOPHAGEAL FISTULA AND OESOPHAGEAL ATRESIA:
AN ANALYSIS OF CLUSTERS
Epidemiologic Patterns of the Malformation
Research and management programs have had notable successes in solving many
problems associated with birth defects; however, the origin or causes of several defects
remain a mystery. Congenital tracheoesophageal fistula (TEF) and oesophageal atresia
(0A) are two such conditions whose etiology is not understood.
TEF is an abnormal passage between the trachea and the esophagus. It assumes any
of a large number of possible forms and is often characterized by a spectrum of symptoms
including choking, problems with swallowing and even death in a large percentage of
cases. 0A is a congenital lack of continuity of the esophagus and is characterized by
excessive salivation, gagging, vomiting, cyanosis and dyspnea. TEF and 0A often appear
together and are often studied together as though they were a single entity. We shall
follow this precedent if for no other reason than to amass enough cases.
Knox (1,2) presented some data that suggest that cases of TEF and 0A occur in
clusters over time. By considering the monthly and annual number of cases admitted to
hospitals in Birmingham, England from 1950 to 1955 and in the Newcastle region from
1950 to 1958, one finds years in which the incidence of reported cases was far in excess
of that of the surrounding years. However, it is less clear that a particular month
repeatedly was associated with a high reported rate. Babbott and Ingalls (3) found a
similar pattern in Pennsylvania County for the period 1951 through 1958, despite rela-tively
uniform birth rates. Koop (h) , in his experience with over 300 infants treated
for 0A in a 15 _ year period in Philadelphia, found that cases of 0A were admitted fairly
consistently over the years in bunches in April; this suggests a seasonal effect. He
reported that on one occasion in a period of 21 days, 17 infants with 0A were admitted
to the Neonatal Unit and that over half of these came from the same area of Pennsylvania
countryside. Other physicians have reported to us that the incidence of 0A and TEF seems
to be greater in April or May. Also, see the paper by Slater et al (5).
Contrary to this, there have been reports of the absence of clustering in time
or space of 0A. There are indeed times and places where clustering is absent but this
could simply reflect that a sporadically-behaved cause is absent as is true of infectious
diseases or it could imply an insensitive data-collecting mechanism. For example, we
have found that data from death certificates regarding certain malformations suggest
disparate conclusions about patterns of the disease depending on whether the condition
is listed as the underlying cause of death or simply mentioned at all.
Also, it is possible that a direct link may be found between a specific malfor-mation
as reflected in data comprised of underlying causes of death (with no or few
other conditions mentioned) and a specific environmental factor (e.g., influenza) and,
further, that this link may be obscured by including in the data deaths for which the
malformation is simply ment i oned . Conceivably, such a mention may be only a snail part
of a constellation of several anomalies associated with the infant, a constellation
caused by different factors (e.g., thalidomide, rubella).

N. C.
Doc.
J-£ NORTH CAROLINA STATE LIBRARY
40?/<3:S4 RALEIGH
" PHSB STUDIES — A Special Report Series by the N,C. Department of Human Resources, Division of
Health Services, Public Health Statistics Branch, P.O. Box 2091, Raleigh, N.C.
No. ]k March 1979
ASSOCIATION OF INFLUENZA WITH CONGENITAL
TRACHEOESOPHAGEAL FISTULA AND OESOPHAGEAL ATRESIA:
AN ANALYSIS OF CLUSTERS
Epidemiologic Patterns of the Malformation
Research and management programs have had notable successes in solving many
problems associated with birth defects; however, the origin or causes of several defects
remain a mystery. Congenital tracheoesophageal fistula (TEF) and oesophageal atresia
(0A) are two such conditions whose etiology is not understood.
TEF is an abnormal passage between the trachea and the esophagus. It assumes any
of a large number of possible forms and is often characterized by a spectrum of symptoms
including choking, problems with swallowing and even death in a large percentage of
cases. 0A is a congenital lack of continuity of the esophagus and is characterized by
excessive salivation, gagging, vomiting, cyanosis and dyspnea. TEF and 0A often appear
together and are often studied together as though they were a single entity. We shall
follow this precedent if for no other reason than to amass enough cases.
Knox (1,2) presented some data that suggest that cases of TEF and 0A occur in
clusters over time. By considering the monthly and annual number of cases admitted to
hospitals in Birmingham, England from 1950 to 1955 and in the Newcastle region from
1950 to 1958, one finds years in which the incidence of reported cases was far in excess
of that of the surrounding years. However, it is less clear that a particular month
repeatedly was associated with a high reported rate. Babbott and Ingalls (3) found a
similar pattern in Pennsylvania County for the period 1951 through 1958, despite rela-tively
uniform birth rates. Koop (h) , in his experience with over 300 infants treated
for 0A in a 15 _ year period in Philadelphia, found that cases of 0A were admitted fairly
consistently over the years in bunches in April; this suggests a seasonal effect. He
reported that on one occasion in a period of 21 days, 17 infants with 0A were admitted
to the Neonatal Unit and that over half of these came from the same area of Pennsylvania
countryside. Other physicians have reported to us that the incidence of 0A and TEF seems
to be greater in April or May. Also, see the paper by Slater et al (5).
Contrary to this, there have been reports of the absence of clustering in time
or space of 0A. There are indeed times and places where clustering is absent but this
could simply reflect that a sporadically-behaved cause is absent as is true of infectious
diseases or it could imply an insensitive data-collecting mechanism. For example, we
have found that data from death certificates regarding certain malformations suggest
disparate conclusions about patterns of the disease depending on whether the condition
is listed as the underlying cause of death or simply mentioned at all.
Also, it is possible that a direct link may be found between a specific malfor-mation
as reflected in data comprised of underlying causes of death (with no or few
other conditions mentioned) and a specific environmental factor (e.g., influenza) and,
further, that this link may be obscured by including in the data deaths for which the
malformation is simply ment i oned . Conceivably, such a mention may be only a snail part
of a constellation of several anomalies associated with the infant, a constellation
caused by different factors (e.g., thalidomide, rubella).